textLarge conductance calcium-activated potassium channels have been shown to be
potentiated by physiologically relevant acute doses of ethanol. Here I show that ethanol
sedation increased transcription of the slowpoke gene, which encodes a largeconductance
calcium-activated potassium channel, in the nervous system of the fruit fly
Drosophila melanogaster, six hours after ethanol sedation. Twenty-four hours after
sedation, neural slowpoke expression was decreased. Sedation with ethanol also induced
tolerance that developed within four hours of sedation and persisted for at least seven
days. Drosophila lacking slowpoke expression only in the nervous system were unable to
acquire tolerance and flies which over-expressed slowpoke displayed resistance to the
sedating effects of ethanol. The expression of several other ion channels was also
increased six hours after ethanol sedation, however no other ion channel mutant tested
showed a deficit in the capacity to acquire tolerance. Wild-type and slowpoke mutant flies
showed no differences in ethanol metabolism following ethanol sedation that could
account for the tolerance or lack of it. Therefore the slowpoke gene appears to play a
unique role in the phenomenon of tolerance.Institute for Cellular and Molecular Biolog
